Correlation of brain blood flow, intracellular pH and metabolism in hypoglycemic cats under halothane and barbiturate anesthesia.
The neurophysiological alterations associated with transient insulin-induced hypoglycemia were compared in 14 cats anesthetized with halothane and 14 cats anesthetized with pentobarbital fasted for 18 h prior to the study. Each anesthetic group was further divided into acute and chronic preparations which in turn were prepared and studied in an identical manner except for the anesthetic agent employed. In the chronic animals there was no difference in survival between the two groups following a 2-h period of hypoglycemia. In these preparations there were no significant differences in: blood glucose levels, mean arterial blood pressure (MABP); arterial carbon dioxide tension (paCO2), arterial oxygen tensions (paO2), arterial pH (pHa), or acid-base balance during the period of hypoglycemia. Differences in the electroencephalograms were commensurate with the anesthetic used. In the acute preparations cerebral blood flow (CBF), xenon-133 clearance technique; brain pH, pH sensitive fluorescent indicator method; and cerebral metabolic rates of oxygen (CMRO2) and glucose consumption were determined at 15-min intervals in addition to the measurements recorded in the chronic group. During a 3-h period of regular insulin administration at a rate of 30 units/kg/h there were no significant differences in any of the systemic or brain measurements recorded except for CBF (halothane greater than barbiturate). EEGs in the acute group of animals paralleled the chronic group and improved but did not return to normal following glucose resuscitation at the end of the period of hypoglycemia. All the acute animals had a normal paCO2-CBF response curve prior to the insulin administration. CBF and brain pH remained constant during the period of hypoglycemia in both groups. However, following the administration of glucose there was a significant brain acidosis and EEG change without a change in CBF. We conclude that: the protective effects of barbiturates in states of hypoxemia or ischemia do not extend to hypoglycemia, brain pH and blood flow are not altered by moderate (as opposed to severe) hypoglycemia, and brain pH may not be the prime regulator in the CBF-metabolic blood flow couple.
D000136:Acid-Base Equilibrium / Q000187:drug effects*; D000768:Anesthesia, General; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D002415:Cats; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects; D006221:Halothane / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D010424:Pentobarbital / Q000494:pharmacology*
D001786:Blood Glucose; D007328:Insulin; D002245:Carbon Dioxide; D010424:Pentobarbital; D006221:Halothane